CACAPIT, LOVELY ROSE S.

OCT 22, 2020

NDA NCENH06

PATHOPHYSIOLOGY OF DIABETIC KETOACIDOSIS

A. SCHEMATIC

LACK OF INSULIN

-DECREASED UTILIZATION OF
GLUCOSE BY MUSCLE, FAT, AND
LIVER INCREASED BREAKDOWN
OF FAT
-INCREASED PRODUCTION OF
GLUCOSE BY LIVER

HYPERGLYCEMIA INCREASED FATTY ACIDS

INCREASED KETONE
BLURRED VISSION POLYURIA
BODIES

- Acetone breath
DEHYDRATION - Poor appetite ACIDOSIS
- Nausea

- Nausea
- Increased thirst - Weakness Increasingly rapid
- Vomiting
(POLYDIPSIA) - Headache respirations
- Abdominal pain
B. NARRATIVE

Without insulin, the amount of glucose entering the cells is reduced, and
production and release of glucose by the liver (gluconeogenesis) is increased,
leading to hyperglycemia. Body will attempt to get rid of the excess glucose, the
kidneys excrete the glucose along with water and electrolytes. This osmotic
diuresis, which is characterized by excessive urination (polyuria), leads to
dehydration and marked electrolyte loss.
Another effect of insulin deficiency is the breakdown of fat (lipolysis) into
free fatty acids and glycerol. The free fatty acids are converted into ketone
bodies by the liver. Ketone bodies are acids; their accumulation in the circulation
due to lack of insulin leads to metabolic acidosis.
Other potential causes of decreased insulin include patient error in
injecting insulin, intentional skipping of insulin doses, or equipment problems.
Illness and infections are associated with insulin resistance. In response to
physical and emotional stressors, there is an increase in the level of “stress”
hormones which are glucagon, epinephrine, norepinephrine, cortisol, and growth
hormone. These hormones promote glucose production by the liver and interfere
with glucose utilization by muscle and fat tissue, counteracting the effect of
insulin. If insulin levels are not increased during times of illness and infection,
hyperglycemia may progress to DKA.

References
Cheever, J. L. (n.d.). Brunner & Suddarth's Textbook of Medical-Surgical Nursing 13th Edition.